Peroxides and free radicals produced by oxidation of unsaturated fatty acids impair the flavor and the nutritive value of food so that a deterioration in quality occurs, for example. Moreover, such peroxides and free radicals cause damage to proteins and DNA in cells due to strong oxidizing power, and cause damage to lipids that form cell membranes to produce highly toxic lipid peroxides (e.g., hydroperoxides) so that cellular damage or tissue damage occurs. It has been revealed that accumulation of adverse effects of active oxygen and free radicals on the living body promotes aging and causes lifestyle-related diseases including cancer, arteriosclerosis, and heart disease. In particular, since lifestyle-related disease is closely related to diet, the importance of improvement in diet on disease prevention has attracted attention. Therefore, research on the relationship between the antioxidative properties of food and food ingredients and research on antioxidative ingredients have been conducted from the viewpoint of preventing or suppressing oxidative stress due to food ingredients.
Plant-derived vitamins, polyphenols, and the like have been known as antioxidative ingredients. Various reports on antioxidative vitamins have been made. In particular, it has been confirmed that vitamin C, vitamin E, β-carotene, and the like have antioxidative properties. Regarding polyphenols, it has been revealed that catechins, flavonoids, and the like have strong antioxidative properties. Various antioxidative peptides have been isolated and identified from protease hydrolyzates of proteins. Three antioxidative peptides have been isolated from an enzymatic decomposition product of egg albumin (see Non-patent Document 1, for example). Six antioxidative peptides have been isolated and identified from a protease hydrolyzate of β-conglycinin (soybean protein) (see Non-patent Document 2, for example).
Enzymatic decomposition products of milk proteins have physiological activities such as an opioid activation effect, a calcium resorption promotion effect, a cell growth effect, an antibacterial effect, and an angiotensin I-converting enzyme inhibitory effect. A method that emulsifies eicosapentaenoic acid-containing oils and fats such as fish oil using a water-soluble protein solution to suppress fish oil odor (see Patent Document 1, for example), and a method that emulsifies highly unsaturated fatty acid-containing oils and fats using a partial hydrolyzate of milk to obtain a powder of the highly unsaturated fatty acid-containing oils and fats with high oxidation stability (see Patent Document 2, for example) have been disclosed. A method that emulsifies highly unsaturated fatty acid-containing oils and fats, cheese, and water to prepare an antioxidative emulsified product to prevent oxidation of the highly unsaturated fatty acid-containing oils and fats and prevent fish odor from highly unsaturated fatty acid-containing fish oils and fats and a foul smell during storage has also been disclosed (see Patent Document 3, for example). The emulsified products of highly unsaturated fatty acid-containing oils and fats disclosed in the above documents are prepared by adding a water-soluble protein solution, a partial hydrolyzate of milk, or cheese to highly unsaturated fatty acid-containing oils and fats, and emulsifying the mixture. The above-mentioned methods prevent fish odor from the highly unsaturated fatty acid-containing fish oils and fats and afoul smell during storage. However, only a few reports have been made that a milk protein-derived peptide has antioxidative properties without mixing a peptide with highly unsaturated fatty acid-containing oils and fats and emulsifying the mixture. The inventors of the present invention have found that a water-soluble peptide fraction of cheese has antioxidative properties, and applied for a patent (see Patent Document 4). The inventors have also found that a peptide having a specific amino acid sequence has antioxidative properties (see Patent Document 5). However, these peptides are mainly contained in mold-ripened cheese. The worldwide production and consumption of lactic acid bacteria-ripened cheese are significantly higher than those of mold-ripened cheese. Lactic acid bacteria-ripened cheese is also utilized as a raw material for processed cheese. Therefore, it is desirable to isolate a peptide component having high antioxidative properties from lactic acid bacteria-ripened cheese.
As described above, accumulation of adverse effects of active oxygen and free radicals on the living body causes lifestyle-related diseases. It is important to prevent risk factors (e.g., hypertension, hyperlipemia, and diabetes) relating to the onset and progression of lifestyle-related disease. In Japan, the number of deaths caused by cardiovascular disease and cerebrovascular disease has increased year by year. Cardiovascular disease and cerebrovascular disease are responsible for about one-third of all deaths. Therefore, measures against cardiovascular disease and cerebrovascular disease have become important issues. The risk of these arteriosclerotic diseases increases significantly due to a combination of risk factors such as hypertension, hyperlipemia, and glucose intolerance. A combination of such risk factors is referred to as metabolic syndrome that has been widely recognized.
It is considered that prevention of excessive visceral fat accumulation is important in order to prevent metabolic syndrome. A fat tissue (i.e., a secretory tissue predominant in a living body) produces various endocrine factors, and is involved in the maintenance of homeostasis of a living body. However, excessive visceral fat accumulation breaks down the secretion balance between the endocrine factors and causes various pathological conditions. A fat tissue has been merely considered to be an energy storage. In recent years, the importance of a fat tissue has attracted attention when considering metabolic disorder syndrome including lifestyle-related disease. Specifically, a fat tissue produces endocrine factors such as a plasminogen activator inhibitor, a tumor necrosis factor (TNF-α), leptin, and adiponectin, and contributes to the maintenance of homeostasis of a living body. It has been revealed that imbalance between the endocrine factors (e.g., excessive production or underproduction) is closely related to the onset and progression of sugar/lipid metabolism disorder, hypertension, and arteriosclerosis.
Adiponectin that is an endocrine factor produced by a fat tissue is a 30 kDa hormone formed of 244 amino acids. It is considered that adiponectin has an effect of suppressing arteriosclerosis and an effect of promoting fat burning in the liver and muscle. Adiponectin has an effect of promoting incorporation of glucose and fatty acid in blood into cells. When fat is accumulated in the muscle, liver, and the like, incorporation of sugar deteriorates so that diabetes may occur. It is considered that adiponectin decomposes fat and sugar that are temporarily accumulated excessively to keep the nutrient balance in the body. The function of adipocytes that secrete adiponectin weakens with the progression of obesity so that the nutrient balance in the body is lost.
Adiponectin specifically secreted by a fat tissue is normally contained in blood at a high level. The adiponectin level decreases due to visceral fat accumulation. Adiponectin has various physiological functions such as preventing diabetes, arteriosclerosis, inflammation, and hypertension. It is very important to promote an increase in blood adiponectin level or suppress a decrease in blood adiponectin level in order to treat metabolic syndrome.
Drug therapy has been employed as measures to treat each pathological condition involved in metabolic syndrome. However, drug therapy requires a prescription and causes side effects. Even if one pathological condition is treated, a serious pathological condition may occur due to other pathological conditions. Therefore, it is necessary to regulate the balance between the endocrine factors produced by a fat tissue. A change in lifestyle is considered to be important (i.e., exercise therapy or diet therapy rather than drug therapy) in order to prevent or treat metabolic syndrome caused by visceral fat accumulation. Therefore, a food or drink that is effective for treating metabolic syndrome caused by visceral fat accumulation and can be taken safely and daily over a long time has been desired.
In recent years, research on food ingredients having a function of suppressing the progression of disease as much as possible through diet has attracted attention rather than treatment using a synthetic medicine.
Adiponectin is known to have a liver fibrosis inhibition effect, a normal hepatocyte growth promotion effect, and an anti-inflammatory effect (see Patent Document 6, for example). As an adiponectin production promoter, a composition that contains a fermented tea extract as an active ingredient (see Patent Document 7, for example), and a blood fat tissue-specific secretion protein enhancement composition that contains an extract of a deciduous sub-canopy tree (Phyllanthus embilica) that belongs to Phyllanthus urinaria (see Patent Document 8, for example) have been disclosed.
On the other hand, cheese is a high-fat-containing food, but has a blood triglyceride level decrease promotion effect and a cholesterol metabolism improvement effect (see Patent Documents 9 and 10). However, no document teaches or suggests that cheese promotes an increase in blood adiponectin level or suppresses a decrease in blood adiponectin level.    Patent Document 1: JP-A-60-102168    Patent Document 2: JP-A-2-305898    Patent Document 3: JP-A-7-274823    Patent Document 4: JP-A-2004-352958    Patent Document 5: JP-A-2005-294358    Patent Document 6: JP-A-2000-256208    Patent Document 7: JP-A-2002-363094    Patent Document 8: JP-A-2006-56836    Patent Document 9: JP-A-2003-300890    Patent Document 10: JP-A-2003-144090    Non-patent Document 1: Tsuge, N et al., Nippon Nogeikagaku Kaishi, 65, p. 1635, 1991    Non-patent Document 2: Chen, H. M. et al., J. Agric. Food Chem., 43, p. 574, 1995